Mechanical signals control SOX-9, VEGF, and c-Myc expression and cell proliferation during inflammation via integrin-linked kinase, B-Raf, and ERK1/2-dependent signaling in articular chondrocytes.

Introduction: The importance of mechanical signals in normal and inflamed cartilage is well established. Chondrocytes respond to changes in the levels of proinflammatory cytokines and mechanical signals during inflammation. Cytokines like interleukin (IL)-1beta suppress homeostatic mechanisms and inhibit cartilage repair and cell proliferation.

Correlation of tuned aperture computed tomography with conventional computed tomography for evaluation of osseous healing in calvarial defects.

Objective: To compare the diagnostic efficacy of iteratively restored tuned aperture computed tomography (TACT) with conventional computed tomography (CT) for evaluation of osseous healing in induced calvarial defects.

Study Design: Fifty-six calvarial defects in 14 rabbits received 1 of 4 possible treatments: copolymer membranes with and without bone marrow stromal cells (BMSCs), BMSCs alone, or no treatment (control). Healing was measured after 2, 4, and 8 wks as remaining defect areas measured on TACT and CT images.

Anti-inflammatory effects of continuous passive motion on meniscal fibrocartilage.

Motion-based therapies have been applied to promote healing of arthritic joints. The goal of the current study was to determine the early molecular events that are responsible for the beneficial actions of motion-based therapies on meniscal fibrocartilage. Rabbit knees with Antigen-Induced-Arthritis (AIA) were exposed to continuous passive motion (CPM) for 24 or 48 h and compared to immobilized knees.

Role of NF-kappaB transcription factors in antiinflammatory and proinflammatory actions of mechanical signals.

Objective: The mechanisms by which chondrocytes convert biomechanical signals into intracellular biochemical events are not well understood. In this study, we sought to determine the intracellular mechanisms of the magnitude-dependent actions of mechanical signals.

Methods: Chondrocytes isolated from rabbit articular cartilage were grown on flexible membranes.

Cleavage of CD14 and LBP by a protease from Prevotella intermedia.

Periodontitis is an inflammatory disease caused by subgingival microorganisms and their components, such as lipopolysaccharide (LPS). Responses of the host to LPS are mediated by CD14 and LPS-binding protein (LBP). In this study, it was determined that proteases from a periodontal pathogen, Prevotella intermedia, cleave CD14 and LBP, and thereby modulate the virulence of LPS.

Signal transduction by mechanical strain in chondrocytes.

Purpose Of Review: Exercise and passive motion exert reparative effects on inflamed joints, whereas excessive mechanical forces initiate cartilage destruction as observed in osteoarthritis. However, the intracellular mechanisms that convert mechanical signals into biochemical events responsible for cartilage destruction and repair remain paradoxical. This review summarizes how signals generated by mechanical stress may initiate repair or destruction of cartilage.

A central role for the nuclear factor-kappaB pathway in anti-inflammatory and proinflammatory actions of mechanical strain.

Mechanical signals play an integral role in bone homeostasis. These signals are observed at the interface of bone and teeth, where osteoblast-like periodontal ligament (PDL) cells constantly take part in bone formation and resorption in response to applied mechanical forces. Earlier, we reported that signals generated by tensile strain of low magnitude (TENS-L) are antiinflammatory, whereas tensile strain of high magnitude (TENS-H) is proinflammatory and catabolic.

Vascularization and tissue infiltration of a biodegradable polyurethane matrix.

Urethanes are frequently used in biomedical applications because of their excellent biocompatibility. However, their use has been limited to bioresistant polyurethanes. The aim of this study was to develop a nontoxic biodegradable polyurethane and to test its potential for tissue compatibility.

Altered Neutrophil Function in Localized Juvenile Periodontitis: Intrinsic or Induced?

Localized juvenile periodontitis (LJP) is an aggressive periodontal disease of familial nature. Neutrophils from a majority of patients with this disease exhibit decreased Chemotaxis with increased adherence, oxidative burst, and degranulation in response to opsonized bacteria. It is proposed that the biological basis for these altered neutrophil functions in LJP may be due either to intrinsic cell abnormalities or to the effect of factors present in the sera of LJP patients, which can modulate neutrophil functions.

The fine structure of early tooth formation in an lguanid lizard, Anolis carolinensis.

Cytodifferentiation and hard tissue formation were studied in Anolis to collect information regarding the phylogenetic history of enamel and the functional significance of the events seen in the mammalian tooth during differentiation. The differentiation of the ameloblasts of Anolis, like that of mammals, shows two phases: In the early phase, the cells are short and rich in free ribosomes, in the late phase the cells elongate, develop an extensive rough endoplasmic reticulum, and the Golgi apparatus moves into that part of the cell next to the basal lamina (the cell apex). The early epithelial-mesenchymal interface resembles that of mammals, suggesting that early mechanisms of induction and epithelial-mesenchymal interaction are similar in Anolis and in mammals.